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2 results on '"Musa, Moji G."'

1. Developmental conditioning of endothelium-derived hyperpolarizing factor-mediated vasorelaxation

Author

Stead, Rebecca, Musa, Moji G., Bryant, Claire L., Lanham, Stuart A., Johnston, David A., Reynolds, Richard, Torrens, Christopher, Fraser, Paul A., and Clough, Geraldine F.

Subjects
maternal obesity, intermediate conductance calcium-activated potassium channels, endothelium derived hyperpolarizing factor, developmental conditioning, microvasculature
Abstract

OBJECTIVES: The endothelium maintains vascular homeostasis through the release of endothelium-derived relaxing factors (EDRF) and endothelium-derived hyperpolarization (EDH). The balance in EDH : EDRF is disturbed in cardiovascular disease and may also be susceptible to developmental conditioning through exposure to an adverse uterine environment to predispose to later risk of hypertension and vascular disease.METHODS: Developmentally conditioned changes in EDH : EDRF signalling pathways were investigated in cremaster arterioles (18-32 μm diameter) and third-order mesenteric arteries of adult male mice offspring of dams fed either a fat-rich (high fat, HF, 45% energy from fat) or control (C, 10% energy from fat) diet. After weaning, offspring either continued on high fat or were placed on control diets to give four dietary groups (C/C, HF/C, C/HF, and HF/HF) and studied at 15 weeks of age.RESULTS: EDH via intermediate (IKCa) and small (SKca) conductance calcium-activated potassium channels contributed less than 10% to arteriolar acetylcholine-induced relaxation in in-situ conditioned HF/C offspring compared with ∼60% in C/C (P CONCLUSION: This is the first evidence that EDH-mediated microvascular relaxation is susceptible to an adverse developmental environment through down-regulation of the IKCa signalling pathway. Conditioned offspring exposed to a 'second hit' (HF/HF) exhibit adaptive vascular mechanisms to preserve dilator function.

Published
2016
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2. PCSK9 Inhibitors: From Nature's Lessons to Clinical Utility.

Author

Raal FJ, Chilton R, Ranjith N, Rambiritch V, Leisegang RF, Ebrahim IO, Tonder AV, Shunmoogam N, Bouharati C, Musa MG, Karamchand S, Naidoo P, and Blom DJ

Subjects
Animals, Atherosclerosis epidemiology, Atherosclerosis prevention & control, Cardiovascular Diseases epidemiology, Cardiovascular Diseases prevention & control, Ezetimibe therapeutic use, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Hypercholesterolemia drug therapy, Hypercholesterolemia epidemiology, Hypolipidemic Agents classification, Hypolipidemic Agents pharmacology, Hypolipidemic Agents therapeutic use, PCSK9 Inhibitors
Abstract

Background: Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors are a novel class of non-statin lipid lowering therapy that reduce LDL-cholesterol by 50 - 60%. PCSK9 inhibitors decrease LDL-cholesterol by preventing intracellular degradation of LDL receptors; subsequently, a greater number of LDL-receptors are available on the cell surface to extract circulating LDL., Objective: To describe the origins of PCSK9 inhibitors and their current use in clinical practice., Methods: We performed a narrative review of the PCSK9 inhibitor class of drugs., Results: Current data indicate that PCSK9 inhibitors effectively reduce LDL-cholesterol and are well tolerated and safe. PCSK9 inhibitors have also been shown to reduce cardiovascular event rates in patients with stable atherosclerotic cardiovascular disease and in patients with a recent (up to one year) acute coronary syndrome. Given the costs, chronicity of the treatment and the potential budget impact, PCSK9 inhibitors are often limited to patients with the highest absolute risk for major adverse cardiovascular events despite optimal treatment with high-intensity statin and ezetimibe., Conclusion: PCSK9 inhibitors have a favorable safety, efficacy and tolerability profile. Postmarketing safety surveillance and real-world studies are needed to further support the long-term safety profile of this class of medicine., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Published
2020
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